Cardiovascular diseases are the first leading cause of death and morbidity in developed countries. The use of animal models have contributed to increase our knowledge, providing new approaches focused to improve the diagnostic and the treatment of these pathologies. Several models have been developed to address cardiovascular complications, including atherothrombotic and cardiac diseases, and the same pathology have been successfully recreated in different species, including small and big animal models of disease. However, genetic and environmental factors play a significant role in cardiovascular pathophysiology, making difficult to match a particular disease, with a single experimental model. Therefore, no exclusive method perfectly recreates the human complication, and depending on the model, additional considerations of cost, infrastructure, and the requirement for specialized personnel, should also have in mind. Considering all these facts, and depending on the budgets available, models should be selected that best reproduce the disease being investigated. Here we will describe models of atherothrombotic diseases, including expanding and occlusive animal models, as well as models of heart failure. Given the wide range of models available, today it is possible to devise the best strategy, which may help us to find more efficient and reliable solutions against human cardiovascular diseases.
Purpose Cardiac magnetic resonance fingerprinting (cMRF) has been recently introduced to simultaneously provide T1, T2, and M0 maps. Here, we develop a 3‐point Dixon‐cMRF approach to enable simultaneous water specific T1, T2, and M0 mapping of the heart and fat fraction (FF) estimation in a single breath‐hold scan. Methods Dixon‐cMRF is achieved by combining cMRF with several innovations that were previously introduced for other applications, including a 3‐echo GRE acquisition with golden angle radial readout and a high‐dimensional low‐rank tensor constrained reconstruction to recover the highly undersampled time series images for each echo. Water–fat separation of the Dixon‐cMRF time series is performed to allow for water‐ and fat‐specific T1, T2, and M0 estimation, whereas FF estimation is extracted from the M0 maps. Dixon‐cMRF was evaluated in a standardized T1–T2 phantom, in a water–fat phantom, and in healthy subjects in comparison to current clinical standards: MOLLI, SASHA, T2‐GRASE, and 6‐point Dixon proton density FF (PDFF) mapping. Results Dixon‐cMRF water T1 and T2 maps showed good agreement with reference T1 and T2 mapping techniques (R2 > 0.99 and maximum normalized RMSE ~5%) in a standardized phantom. Good agreement was also observed between Dixon‐cMRF FF and reference PDFF (R2 > 0.99) and between Dixon‐cMRF water T1 and T2 and water selective T1 and T2 maps (R2 > 0.99) in a water–fat phantom. In vivo Dixon‐cMRF water T1 values were in good agreement with MOLLI and water T2 values were slightly underestimated when compared to T2‐GRASE. Average myocardium septal T1 values were 1129 ± 38 ms, 1026 ± 28 ms, and 1045 ± 32 ms for SASHA, MOLLI, and the proposed water Dixon‐cMRF. Average T2 values were 51.7 ± 2.2 ms and 42.8 ± 2.6 ms for T2‐GRASE and water Dixon‐cMRF, respectively. Dixon‐cMRF FF maps showed good agreement with in vivo PDFF measurements (R2 > 0.98) and average FF in the septum was measured at 1.3%. Conclusion The proposed Dixon‐cMRF allows to simultaneously quantify myocardial water T1, water T2, and FF in a single breath‐hold scan, enabling multi‐parametric T1, T2, and fat characterization. Moreover, reduced T1 and T2 quantification bias caused by water–fat partial volume was demonstrated in phantom experiments.
Myocardial infarction and subsequent heart failure is a major health burden associated with significant mortality and morbidity in western societies. The ability of cardiac tissue to recover after myocardial infarction is affected by numerous complex cellular and molecular pathways. Unbalance or failure of these pathways can lead to adverse remodelling of the heart and poor prognosis. Current clinical cardiac imaging modalities assess anatomy, perfusion, function, and viability of the myocardium, yet do not offer any insight into the specific molecular pathways involved in the repair process. Novel imaging techniques allow visualisation of these molecular processes and may have significant diagnostic and prognostic values, which could aid clinical management. Single photon-emission tomography, positron-emission tomography, and magnetic resonance imaging are used to visualise various aspects of these molecular processes. Imaging probes are usually attached to radioisotopes or paramagnetic nanoparticles to specifically target biological processes such as: apoptosis, necrosis, inflammation, angiogenesis, and scar formation. Although the results from preclinical studies are promising, translating this work to a clinical environment in a valuable and cost-effective way is extremely challenging. Extensive evaluation evidence of diagnostic and prognostic values in multi-centre clinical trials is still required.
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